Acutely and recently HIV-l-infected individuals who received suppressive antiviral therapy (highly active antiretroviral therapy, HAART) early in their disease course often develop strong HIV-1 Gag-specific CD4+ T cell proliferative responses, a type of cellular immune response that is generally absent in chronically HIV-infected individuals with progressive disease. Furthermore, many of those acutely infected/treated patients are able to control viral replication and maintain low viral loads off of therapy following a series of structured treatment interruptions (STIs). This control of viral replication is temporally associated with increasing HIV-specific cytotoxic T lymphocyte (CTL) responses. These findings suggest that there might be a relationship between HIV-specific helper T lymphocyte (HTL) and CTL responses and the ability to control viral replication in vivo in the acute infection setting, and even that strong HIV-specific cellular immune responses might predict immunologic control of viral replication. However, the frequency, diversity of epitope recognition, and the function of HIV-1-specific CD4+ T cells in acutely-infected and early treated individuals has not been fully evaluated. Furthermore, the relationship between HTL and CTL responses in this setting, their ability to exert immune selection pressure on replicating HIV-1, and their role in controlling viremia in this clinical setting has likewise not been prospectively and comprehensively studied. Therefore, to address these issues, we specifically propose: 1) To characterize HIV-1-specific HTL and CTL responses in HAART-treated and untreated seroconverters and assess the relationship between HIV-1-specific HTL and CTL responses, 2) To determine which features of HIV-specific HTL and CTL responses following vaccination predict subsequent virologic control following STI in a subset of acutely-infected, HAART-treated patients who choose to receive therapeutic vaccination followed by structured treatment interruption (STI), and 3) To determine whether viral mutations that arise during STI suggest evidence of immune selection pressure mediated by either HIV-specific CD4+ or CD8+ T cells, and whether viral escape from HTL or CTL recognition plays a role in failure to control viral replication during STI in the acutely-infected, HAART-treated, vaccinated cohort.